Верэсяловыя кусточкі

Верэсяловыя кусточки / Не ламаўшы храскают. / Ой, цеперашныя мальцы, / Не любиўшы, хвастаю

Climate change in Nepal:a comprehensive analysis of instrumental data and people’s perceptions

Despite broad scientific consensus on climate change, public views may not always correspond with scientific findings. Understanding public perceptions of climate change is thus crucial to both identifying problems and delivering solutions. Investigations of climate change that integrate instrumental records and people’s perceptions in the Himalayas are scarce and fragmentary compared to other regions of the world. We analyzed nationally representative data (n = 5060) of local peoples’ perception of climate change in Nepal, and assessed annual and seasonal trends of temperature and precipitation, onsets of seasons, and trends of climate extremes, based on gridded climate datasets. We firstly used quantitative and spatial techniques to compare local perceptions and the instrumentally observed trends of climate variables. We then examined the possible association of demographic variables, place attachment, regional differences, and prior understanding of climate change with the accuracy of people’s perceptions. Instrumental evidence showed consistent warming, increasing hot days and nights, and increasing annual precipitation, wet spells, heavy precipitation and decreasing dry spells in Nepal. Our results indicate that locals accurately perceived the shifts in temperature but their perceptions of precipitation change did not converge with the instrumental records. We suggest that, in future as exposure to changes in weather, particularly extreme events, continues, people may become more likely to detect change which corresponds with observed trends. With some new methodological insights gained through integrating community perceptions with observed climate data, the results of this study provides valuable information to support policies to reduce climate-related risk and enhance climate change adaptation

Neuroprotective effects of antidepressants via upregulation of neurotrophic factors in the MPTP model of Parkinson's disease

Neurotrophic factors are essential for neuronal survival, plasticity, and development and have been implicated in the action mechanism of antidepressants. In this study, we assessed the neurotrophic factor-inducing and neuroprotective properties of antidepressants. In the first part of the study, we found that fluoxetine, imipramine, and milnacipran (i.p., 20 mg/kg/day for 1 week or 3 weeks) upregulated brain-derived neurotrophic factor in the striatum and substantia nigra both at 1 week and 3 weeks. In contrast, an increase in the glial-derived neurotrophic factor was more obvious at 3 weeks after the antidepressants treatment. Specifically, it was found that fluoxetine and imipramine are more potent in raising the levels of neurotrophic factors than milnacipran. Furthermore, antidepressants elevated the phosphorylation of extracellular signal-regulated-protein kinase (ERK1/2) and the serine/threonine kinase Akt. In the second part of the study, we compared the neuroprotective effects of fluoxetine, imipramine, and milnacipran in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model of Parkinson's disease. Pretreament with fluoxetine, imipramine or milnacipran for 3 weeks reduced MPTP-induced dopaminergic neurodegeneration and microglial activation in the nigrostriatal pathway. Neurochemical analysis by HPLC exhibited that antidepressants attenuated the depletion of striatal dopamine. In consistent, beam test showed that behavioral impairment was ameliorated by antidepressants. Neuroprotective effects were more prominent in the fluoxetine or imipramine treatment group than in milnacipran treatment group. Finally, we found that neuroprotection of the antidepressants against 1-methyl-4-phenylpyridinium neurotoxicity in SH-SY5Y cells was attenuated by ERK or Akt inhibitor. These results indicate that neuroprotection by antidepressants might be associated with the induction of neurotrophic factors, and antidepressant could be a potential therapeutic intervention for treatment of Parkinson's disease

Enhanced dopaminergic neurotoxicity mediated by MPTP in IL-32β transgenic mice

Parkinson's disease (PD) is a neurodegenerative disorder characterized by prominent loss of the nigral dopaminergic neurons and motor symptoms, such as resting tremor and bradykinesia. Evidence suggests that neuroinflammation may play a critical role in PD pathogenesis. Interleukin (IL)-32 is a newly-identified proinflammatory cytokine, which regulates innate and adaptive immune responses by activating p38 MAPK and NF-κB signaling pathways. The cytokine has been implicated in cancers and autoimmune, inflammatory, and infectious diseases. In this study, we attempted to identify the effects of IL-32β on dopaminergic neurotoxicity induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), using IL-32β transgenic mice. Male wild type and IL-32β transgenic mice received intraperitoneal injections of vehicle or MPTP (15\ua0mg/kg\ua0×\ua04). Immunohistochemistry showed that overexpression of IL-32β significantly increased MPTP-mediated loss of dopaminergic neurons in the substantia nigra and deletion of tyrosine hydroxylase-positive fibers in the striatum. Dopamine depletion in the striatum and deficit in locomotor activity were enhanced in IL-32β transgenic mice. These results were accompanied by higher neuroinflammatory responses in the brains of transgenic mice. Finally, we found that IL-32β exaggerated MPTP-mediated activation of p38 MAPK and JNK pathways, which have been shown to be involved in MPTP neurotoxicity. These results suggest that IL-32β exacerbates MPTP neurotoxicity through enhanced neuroinflammatory responses